The physiological characteristics of children′s skin and their growth and development needs determine the particularity of pediatric scar management. However, there were no clinical practice guidelines for the prevention and treatment of pediatric scars worldwide previously. The Clinical Practice Guideline for the Prevention and Treatment of Scars in Children (2025 Edition), released by the Chinese Society of Burn Surgery of the Chinese Medical Association in 2025, is based on evidence-based medicine. Focusing on 10 key clinical issues in pediatric scar prevention and treatment, including wound management, pharmacological therapy, physical therapy, surgical treatment, rehabilitation intervention, and psychological support, the guideline formulates 20 recommendations and establishes an integrated guidance system covering the prevention-treatment-rehabilitation continuum for pediatric scars. Combined with its formulation background and features, the guideline provides detailed literature evidence in the interpretation section of the recommendations, emphasizes the inherent logic behind the development of these recommendations, and conducts a comprehensive and objective evaluation of currently controversial therapeutic methods in clinical practice. It can serve as a practical guide and reference for clinicians to standardize the prevention and treatment of pediatric scars. Based on the research progress in pediatric scar prevention and treatment, this article analyzes the key points of the guideline to facilitate better understanding and implementation.

The identification of biomarkers is essential for developing innovative therapeutic strategies for intervertebral disc degeneration (IVDD). Thioredoxin-interacting protein (TXNIP), a member of the α-arrestin protein family, is modulated by various cellular stress responses and inhibits the antioxidant activity of thioredoxin through direct binding, thereby promoting oxidative stress. Furthermore, TXNIP interacts with nucleotide-binding domain-like receptor protein 3 (NLRP3) to directly activate inflammatory pathways, playing a pivotal role in IVDD progression. IVDD is a common degenerative disorder closely associated with aging, oxidative stress, and chronic inflammation. Currently, there are no effective drugs to reverse its progression. Recent studies have shown that, in degenerated intervertebral discs, TXNIP expression level is closely associated with inflammatory factors, oxidative damage, and cell death, indicating that TXNIP may serve as a central molecular node linking multiple pathological mechanisms in IVDD. This review systematically elucidates the biological functions of TXNIP in oxidative stress, inflammatory activation, metabolic reprogramming, pyroptosis, and apoptosis, as well as its regulatory networks, and summarizes its pivotal role in the occurrence and development of IVDD. Furthermore, from a translational medicine perspective, this review summarizes the current research progress of therapeutic strategies targeting TXNIP, including small-molecule inhibitors, natural compounds, genetic interventions, and biomaterials, and proposes a multimodal therapeutic pathway and clinical translation direction targeting TXNIP, aiming to provide new insights and theoretical foundations for the mechanistic research and targeted treatment of IVDD.

Objective ·To investigate the salivary metabolic characteristics of periodontitis patients with chronic renal failure (CRF) and analyze the role of phosphorus metabolites in this pathological process. Methods ·A total of 45 patients treated at the Department of Nephrology and the Department of Periodontology, Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine were enrolled, including 15 patients with both periodontitis and CRF in the CRF group, 15 with only periodontitis in the periodontitis (CP) group, and 15 in the healthy control (HC) group. All participants underwent unstimulated saliva collection and periodontal clinical examination. Periodontal clinical parameters were recorded, and renal function indicators of patients in the CRF group were documented. Untargeted metabolomic analysis of saliva samples was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Principal component analysis (PCA) was used to analyze inter-group differences and screen differential metabolites. Significantly differential metabolites were further analyzed for pathway enrichment using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. One major differential metabolite was selected for in vitro experiments to verify its effect on osteogenic differentiation of mouse embryonic preosteoblasts MC3T3-E1. Results ·Probing depth (PD), clinical attachment loss (CAL), and plaque index (PI) in the CRF group were significantly higher than those in the CP group (all P<0.05). In the CRF group, urea level (r=0.41) and creatinine level (r=0.61) were positively correlated with PD, and creatinine level was also positively correlated with CAL (r=0.53). Estimated glomerular filtration rate (eGFR) was negatively correlated with PD (r=-0.69) and CAL (r=-0.56), respectively. PCA results showed significant differences in metabolite profiles among the three groups, with phosphoric acid presenting remarkable differences. KEGG analysis revealed that the enriched differential metabolites were mainly involved in protein digestion and absorption, neuroactive ligand-receptor interaction, sphingolipid metabolism, necroptosis, choline metabolism in cancer, ovarian steroidogenesis, sphingolipid signaling, and mineral absorption. In vitro experiments confirmed that 4 mmol/L phosphate ions downregulated the mRNA and protein expression levels of Runt-related transcription factor 2 (Runx2), alkaline phosphatase (Alp), and osteocalcin (Ocn) in MC3T3-E1 cells (all P<0.05), thereby inhibiting osteogenic differentiation. Conclusion ·Periodontal tissue destruction is more severe in periodontitis patients complicated with CRF than those without CRF. Upregulated salivary phosphorus concentration may be one of the mechanisms by which chronic kidney disease aggravates periodontal tissue destruction. Excessively high phosphorus concentration can inhibit osteogenic differentiation.

Objective ·To investigate the effects of bacteria on fibroblast function in vitro and the impact of bacterial intervention on hypertrophic scars in rabbit ears in vivo. Methods ·A total of 16 clinical hypertrophic scar specimens and normal skin tissues were collected from patients admitted to the Department of Burns, Plastic Surgery and Wound Repair, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, from January 2023 to December 2024, and subjected to Gram staining. After amplification and inactivation, standard Staphylococcus aureus was used to treat fibroblasts derived from normal skin at concentrations of 10², 10³, and 10⁴ CFU/mL. The effects on fibroblast proliferation were observed by using Edu staining, while α-smooth muscle actin (α-SMA) expression was detected by immunofluorescence. The expression levels of vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), type Ⅰ collagen and type Ⅲ collagen were measured by Western blotting. Additionally, the secretion of inflammatory cytokines, including interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1), was evaluated by using enzyme-linked immunosorbent assay (ELISA). In the in vivo study, 80 wounds were created on the ears of 10 New Zealand white rabbits, followed by inoculation with Staphylococcus aureus. After hypertrophic scar formation, intradermal injections of levofloxacin or saline were administered. Scar growth was monitored, and Vancouver Scar Scale scores were recorded. Scar tissues were harvested for hematoxylin and eosin staining, Masson staining, and Gram staining, along with immunohistochemical detection of IL-6, IL-8, TNF-α, and MCP-1 expression. Results ·Clinical scar tissues exhibited significantly greater abundance of Gram-positive bacteria than normal skin tissues (P=0.001). In vitro experiments demonstrated that low-abundance bacteria (10² and 10³ CFU/mL) significantly promoted fibroblast proliferation (P=0.045, P=0.017) and α-SMA expression (P=0.042, P=0.002). These bacteria also enhanced the expression of VEGF (P=0.023, P=0.011), TGF-β1 (P=0.029, P=0.031), type Ⅰ collagen (P=0.032, P=0.025), and type Ⅲ collagen (P=0.019, P=0.027), as well as the secretion of inflammatory cytokines IL-6 (P=0.023, P=0.011), IL-8 (P=0.021, P=0.009), TNF-α (P=0.029, P=0.011), and MCP-1 (P=0.023, P=0.008). In the rabbit ear model, levofloxacin injection significantly reduced scar hyperplasia at 45 and 60 days (P=0.019, P=0.013). At 60 days, treated scars showed decreased inflammatory cell infiltration, reduced bacterial load, less collagen deposition, and lower expressions of IL-6 (P=0.025), IL-8 (P=0.021), MCP-1 (P=0.028), and TNF-α (P=0.019). Conclusions ·Low-abundance bacteria promote the profibrotic capacity of scar fibroblasts, while antibiotic application effectively mitigates hypertrophic scar formation.

Objective ·To investigate the effect of apocynin (APO) on periodontitis-induced cognitive impairment in mice and its underlying mechanism. Methods ·C57BL/6 mice were used. A periodontitis model was established by injecting Porphyromonas gingivalis lipopolysaccharide (P.g LPS) into the palatal gingival sulcus of the maxillary first molars twice a week for four weeks. Apocynin was administered intraperitoneally as an intervention. Micro-computed tomography (Micro-CT) was used to observe alveolar bone resorption. The open field test and the Morris water maze were employed to assess cognitive function. Evans blue staining was used to detect blood-brain barrier permeability. Real-time qPCR was used to detect the mRNA expression levels of tight junction proteins zonula occludens-1 (Zo-1) and occludin (Occl), as well as interleukin-1β (Il-1β) and interleukin-8 (Il-8) in brains. Results ·Compared with the P.g LPS group, mice in the P.g LPS plus apocynin group showed significantly increased bone volume fraction (BV/TV) and bone mineral density (BMD), and a significantly decreased bone surface/bone volume ratio (BS/BV). In the open field test, there were no significant differences in locomotor activity among the four groups. In the Morris water maze, the latency of the P.g LPS plus apocynin group was significantly shorter than that of the P.g LPS group from day 3 during the navigation phase. In the probe test, the P.g LPS plus apocynin group crossed the target platform significantly more times than the P.g LPS group. Evans blue staining indicated that the absorbance values decreased significantly in the P.g LPS plus apocynin group. Compared with the P.g LPS group, the expression of Zo-1 (P=0.024) and Ocln (P=0.014) was upregulated, while Il-1β (P=0.001) and Il-8 (P=0.002) were downregulated in the brains of mice treated with apocynin. Conclusion ·Apocynin can alleviate periodontitis-induced cognitive impairment by inhibiting P.g LPS-induced inflammation, reducing alveolar bone resorption, and decreasing blood-brain barrier permeability. These findings suggest that apocynin may have potential neuroprotective effects, which provides an experimental basis for the treatment of periodontitis-related cognitive impairment.

Objective ·To systematically compare the characteristics of long non-coding RNAs (lncRNAs) and their mediated competing endogenous RNA (ceRNA) regulatory networks in periodontitis (PD) and peri-implantitis (PI). Methods ·Twenty-four male SD rats were randomly divided into the control (CON), PD, and PI groups, with eight rats in each group. In the PD group, an experimental PD model was established by ligating the bilateral maxillary first molars with silk sutures. In the PI group, custom titanium implants were placed in the bilateral maxillary first molar regions, followed by silk ligation to induce PI. Gingival tissues from each group were collected for transcriptome sequencing to obtain expression profiles of lncRNAs and mRNAs. DESeq2 was used to screen differentially expressed lncRNAs and mRNAs. Weighted gene co-expression network analysis (WGCNA) was performed to identify module genes associated with PD and PI. Gene Ontology (GO) functional enrichment analysis of the module genes was conducted using KOBAS software. miRNA binding sites were predicted using miRanda software (score≥150), and lncRNA-miRNA-mRNA ceRNA regulatory networks associated with PD- and PI-related module genes were constructed. ceRNA regulatory axes related to PD and PI modules were screened. Results ·Compared with the CON group, 124 up-regulated and 406 down-regulated differentially expressed lncRNAs were identified in the PD group, while 43 up-regulated and 95 down-regulated differentially expressed lncRNAs were identified in the PI group. A total of 22 lncRNAs were differentially expressed in both PD and PI groups. Additionally, 508 lncRNAs were specifically differentially expressed in the PD group, and 116 in the PI group. WGCNA identified the lightcyan module significantly positively correlated with PD and the midnightblue module significantly positively correlated with PI. GO functional enrichment analysis showed that genes in the lightcyan module were significantly enriched in biological processes related to endoplasmic reticulum-associated degradation (ERAD) signaling and response to endoplasmic reticulum stress (ERS), whereas genes in the midnightblue module were significantly enriched in biological processes such as skin barrier formation, keratinocyte differentiation, and epithelial development. Based on these modules, ceRNA regulatory networks were constructed, revealing regulatory axes associated with ERS in the PD group, including ENSRNOG00000063579-miR-1249-Calr (calreticulin), ENSRNOG00000063579-miR-1249-Man1b1 (mannosidase α class 1B member 1), ENSRNOG00000063488-miR-328a-5p-Rnf183 (ring finger protein 183), and ENSRNOG00000063230-miR-3558-5p-Fbxo2 (F-box protein 2), as well as regulatory axes associated with skin barrier function in the PI group, including ENSRNOG00000067449-miR-238a-5p-Krt1 (keratin 1), ENSRNOG00000067449-miR-238a-5p-Krt16, ENSRNOG00000067625-miR-3541-Klf4 (Krüppel-like factor 4), and ENSRNOG00000067625-miR-667-5p-Tgm3 (transglutaminase 3). Conclusion ·This study reveals differences in lncRNA and mRNA expression profiles between PD and PI, suggesting that the two diseases are respectively associated with pathways related to ERS and skin barrier function. These findings provide a basis for understanding the molecular pathological characteristics of the two diseases.

Objective ·To compare the safety outcomes between immunotherapy continuation and permanent immunotherapy discontinuation in patients with lung cancer who developed immune checkpoint inhibitor-associated myocarditis (ICI-M). Methods ·This single-center retrospective cohort study enrolled 357 lung cancer patients who were diagnosed with ICI-M between June 2016 and August 2024 in Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine. Based on post-ICI-M immunotherapy strategies, patients were categorized into a permanent discontinuation group (n=131) and a continuation group (n=226). The continuation group comprised patients who never interrupted immunotherapy and those who temporarily discontinued but later resumed ICI treatment. The ICI-M recurrence rate and the incidence of other new-onset immune-related adverse events (irAEs) were reported. The severity of initial and recurrent ICI-M was compared, and risk factors for ICI-M recurrence or new-onset irAEs were explored. Multivariable Cox regression analysis was used to evaluate the impact of immunotherapy continuation on major adverse cardiovascular events (MACE). Propensity score matching was performed as a sensitivity analysis to enhance the robustness of the study findings. Results ·The ICI-M recurrence rate was 8.8% (20/226). The clinical severity and peak levels of myocardial injury biomarkers were not higher in recurrent ICI-M than in initial ICI-M. A total of 13.3% (30/226) of patients developed other new-onset irAEs. Patients who experienced ICI-M recurrence or new-onset irAEs had a significantly earlier onset of initial ICI-M (47.0 d vs 71.0 d, P=0.006) and a higher peak creatine kinase-MB (CK-MB) level (4.8 ng/mL vs 2.8 ng/mL, P=0.019). Multivariable Cox regression analysis indicated that immunotherapy continuation did not significantly increase the risk of long-term MACE (HR=0.75, 95%CI 0.28‒1.98, P=0.556), and this result remained consistent across all subgroups (P_interaction>0.05). Sensitivity analysis using propensity score matching confirmed the robustness of this result (after matching: HR=0.93, 95%CI 0.32‒2.70, P=0.894). Conclusion ·Continued immunotherapy after ICI-M in lung cancer patients shows an overall favorable safety profile, with a low ICI-M recurrence rate and no significant increase in MACE incidence. This study provides preliminary evidence to support clinical decision-making; however, large-scale prospective studies are still needed for further confirmation and validation.

Objective ·To investigate the genotypic distribution of thalassemia in pregnant women in Nanning, Guangxi, and its impact on pregnancy outcomes. Methods ·A retrospective cohort study was conducted among 3 649 pregnant women enrolled from January 2021 to December 2024 at the Guangxi Zhuang Autonomous Region People′s Hospital. Participants were categorized into α-thalassemia (n=1 296), β-thalassemia (n=505), α-composite β- thalassemia (n=100), and normal controls (n=1 748) based on genetic diagnosis. Hematological parameters, including mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), hemoglobin (Hb), and HbA₂, as well as pregnancy outcomes such as low birth weight (LBW) and preterm birth, were compared among the groups. Multivariate Logistic regression was used to analyze the association between thalassemia genotypes and adverse outcomes. The optimal cut-off values of MCV and HbA₂ for predicting α-composite β-thalassemia were determined using receiver operating characteristic (ROC) curve analysis. Results ·The predominant genotypes were --^SEA/αα (50.62%) in α-thalassemia, βCD41-42/β^N (46.93%) in β-thalassemia, and --^SEA/αα combined with βCD17/β^N (12.00%) in α-composite β-thalassemia. The levels of MCV, MCH, and Hb in the β-thalassemia group were significantly lower than those in the other groups (all P<0.001), while the HbA₂ levels in the β-thalassemia group and the α-composite β-thalassemia group were significantly higher than those in the normal and α-thalassemia groups. The optimal cut-off values for predicting α-composite β-thalassemia were MCV ≤74.95 fL (AUC=0.788) and HbA₂ ≥3.35% (AUC=0.867). β-thalassemia was an independent risk factor for LBW in offspring (aOR=1.785, 95%CI 1.051‒3.031, P=0.032). However, before adjustment for confounding factors, the α-composite β-thalassemia group exhibited the highest risk of LBW (OR=2.592, 95%CI 1.368‒4.912, P=0.004). Conclusion ·Thalassemia genotypes in pregnant women in Nanning, Guangxi, exhibit distinct regional patterns, with β-thalassemia and α-composite β-thalassemia significantly increasing LBW risk. Combined α- and β-thalassemia genetic testing is recommended for pregnant women with MCV ≤74.95 fL and HbA₂≥3.35%, and those with β-thalassemia should be monitored as a high-risk group for LBW.

Objective ·To investigate the value of the T-cell mitochondrial damage index (MDI) in risk prediction for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods ·A total of 100 patients with chronic obstructive pulmonary disease (COPD) who attended the Department of Respiratory Medicine, Jinhua Municipal Central Hospital, from May 2023 to December 2024 were enrolled. According to the post-bronchodilator percentage of predicted forced expiratory volume in 1 second (FEV₁%pred), they were divided into the moderate COPD group (50%≤FEV₁%pred<80%, n=50) and the severe COPD group (30%≤FEV₁%pred<50%, n=50). Additionally, 50 healthy individuals who underwent physical examinations during the same period were included as the healthy control group. Baseline characteristics of all subjects (including general clinical data and laboratory indicators) were collected. Flow cytometry was used to detect and compare the MDI of peripheral blood T cells and their subsets (CD3⁺, CD3⁺CD4⁺, and CD3⁺CD8⁺) in the three groups. The patients with COPD were followed up for 6 months, and were classified into the acute exacerbation (AE) group and the non-AE group according to whether AE occurred during follow-up. Differences in baseline characteristics between the two groups were compared. LASSO regression was used to screen baseline predictors of AECOPD. Univariable and multivariable Logistic regression models were used to establish a predictive model for AECOPD risk, and the performance of the model was validated using the receiver operating characteristic (ROC) curve, calibration curve, and five-fold cross-validation. Results ·The abnormal rates of MDI in T cells and their subsets were higher in patients with COPD than in the healthy control group. Among them, the abnormal rate of CD3⁺CD8⁺ T-cell MDI in the severe COPD group was significantly higher than that in the moderate COPD group and the healthy control group (both P<0.05). After 6 months of follow-up, 46 patients with COPD developed AE. Compared with the non-AE group, the patients in the AE group had lower FEV₁ levels (P<0.001), and higher COPD assessment tests (CAT) scores (P<0.001). Moreover, there were statistically significant differences in the categorical distribution of MDI injury grades in T cells and their subsets between the two groups (all P<0.001), with a higher proportion of mild-to-severe injury observed in the AE group. LASSO regression identified four baseline predictors: CD3⁺ T-cell MDI, CD3⁺CD8⁺ T-cell MDI, FEV₁, and CAT score. The area under the curve (AUC) of the AECOPD risk prediction model constructed based on these four variables was 0.848 (95%CI 0.772—0.923, P<0.001), with a sensitivity of 70.0% and a specificity of 81.0%. The calibration curve showed good model fit (P=0.136), and in the five-fold cross-validation, the accuracies of the training set and validation set was 0.80±0.03 and 0.82±0.06, respectively. Conclusion ·The AECOPD risk prediction model constructed based on CD3⁺ T-cell MDI, CD3⁺CD8⁺ T-cell MDI, FEV₁, and CAT score has good predictive value and may provide a reference for early clinical intervention.

Objective ·Based on preoperative CT imaging combined with clinical indicators, predictive models were constructed to evaluate its application value in the recurrence risk and survival status of patients with hepatocellular carcinoma (HCC) after liver transplantation. The aim was to identify patients who exceeded the Milan criteria but could still obtain an ideal prognosis after liver transplantation, and to provide a new evidence-based basis for optimizing the selection strategy of liver transplant recipients. Methods ·Patients with HCC who underwent first orthotopic liver transplantation at Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, from January 2015 to January 2025 were included. The clinical data, including laboratory examinations, pathological results, and CT imaging were collected. The follow-up period was defined as the time from the date of liver transplantation to patient death or the study endpoint (January 31, 2025). The patients included in the study were evaluated using the Milan criteria, and the distribution of patients who met and exceeded the Milan criteria was analyzed. Through univariate and multivariate Cox analyses, independent risk factors affecting tumor recurrence and overall survival after liver transplantation in patients with HCC were screened, and predictive models for recurrence risk and survival prognosis were constructed. According to the regression coefficient (β) of each variable in the multivariate Cox regression results, proportional scores were assigned. According to the principle of maximizing the Youden index, the optimal cut-off value of the risk score was determined. The patients were divided into low-risk and high-risk groups, and the differences in recurrence-free survival and cumulative survival between the two groups were evaluated. The model risk scores were cross-stratified with the UCSF (University of California, San Francisco) standard to analyze the differences between the recurrence-free survival and cumulative survival among different stratified groups. Results ·A total of 95 patients with HCC were included in the study, among whom 64 exceeded the Milan criteria and 44 had postoperative tumor recurrence. According to the results of multivariate Cox regression analysis, preoperative AFP>400 ng/mL, tumor number>3, maximum tumor diameter>3 cm, and liver-spleen maximum length ratio (LSLR)>1.43 were included to establish the recurrence-free prediction model (P<0.05). Additionally, preoperative AFP>400 ng/mL, tumor number>3, maximum tumor diameter>3 cm, and liver-to-spleen density ratio (LSR)>1.2 were included to establish the survival prediction model (P<0.05). According to the models, the patients were subsequently stratified into low-risk and high-risk groups. In the recurrence-free prediction model, the 1-year, 3-year, and 5-year recurrence-free survival rates (86.2% vs 22.7%, 78.0% vs 6.5%, 78.0% vs 3.2%; χ²=63.642, P<0.001) and cumulative survival rates (87.8% vs 74.2%, 82.8% vs 51.2%, 79.0% vs 25.6%; χ²=14.878, P<0.001) in the low-risk group were significantly higher than those in the high-risk group. In the survival prediction model, the 1-year, 3-year, and 5-year recurrence-free survival rates (82.5% vs 19.8%, 68.7% vs 4.9%, 68.7% vs 4.9%; χ²=55.999, P<0.001) and cumulative survival rates (90.8% vs 67.2%, 83.9% vs 42.2%, 80.4% vs 14.1%; χ²=27.590, P<0.001) in the low-risk group were also significantly higher than those in the high-risk group. In the recurrence-free prediction model and survival prediction model, there were no significant differences in the recurrence-free survival and cumulative survival between the low-risk group within the UCSF criteria and the low-risk group beyond the UCSF criteria. Conclusion ·The recurrence and survival prediction models constructed in this study can effectively evaluate the recurrence risk and survival status of HCC patients after liver transplantation, and can provide a new basis for screening patients who exceed the Milan criteria but still achieve favorable prognosis after liver transplantation, thereby contributing to the optimization of liver transplant recipient selection strategies.

Patients with major depressive disorder commonly exhibit varying degrees of social dysfunction, whose pathological mechanisms may be closely associated with abnormalities in the social reward system.In recent years, research on social reward circuitry has shifted from a focus on localized functional deficits to a systematic perspective of dysregulation across multiple brain regions. Using multimodal neuroimaging and computational modeling approaches, researchers have begun to explore the dynamic interaction patterns between large-scale brain networks and reward circuitry across the three phases of anticipation, consumption, and learning, as well as emerging topics such as circuit-targeted neuromodulation.This review systematically summarizes the functional abnormalities in the social reward circuitry of patients with major depressive disorder, exploring the potential dual mechanisms involving localized functional impairments of key brain regions and network-level dysregulation across three distinct phases of reward processing: anticipation, consumption, and learning, and elaborates the dynamic manifestation of a dual-mechanism model of local brain region functional impairment-network coordination dysregulation during these phases. The review may provide theoretical foundations for understanding the neural substrates underlying social dysfunction in depression and for optimizing clinical treatment strategies, such as precise neuromodulation targeting specific phases or specific circuits.

Endometrial carcinoma (EC) is a common malignant tumor that poses a severe threat to women's health. Driven by an aging population and the high prevalence of metabolic diseases, the incidence of EC continues to rise. For advanced or recurrent EC, traditional therapeutic regimens exhibit limited efficacy and are prone to drug resistance, leading to a generally poor overall prognosis. To overcome this clinical bottleneck, immunotherapeutic strategies, characterized by high targeting specificity and durable efficacy, have opened up a novel direction for clinical treatment. This review systematically summarizes the cellular composition and molecular subtyping characteristics of the EC immune microenvironment, and elaborates on the research progress of immune checkpoint inhibitors (ICIs) in monotherapy and combination regimens. Furthermore, it provides an in-depth analysis of current challenges, including efficacy heterogeneity and drug resistance, to provide a reference for the clinical practice and theoretical research of precision immunotherapy for EC.

Non-syndromic craniosynostosis (NSC) is a common congenital developmental malformation in childhood. It is characterized by the premature fusion of one or more cranial sutures, which in turn leads to abnormal skull morphology, increased intracranial pressure, and a series of neurodevelopmental problems. Depending on the different cranial sutures involved, NSC can present with various abnormal head shapes, such as scaphocephaly, trigonocephaly, anterior plagiocephaly, brachycephaly, and posterior plagiocephaly. Currently, surgical treatment remains the only effective intervention for NSC, aiming to release the fused cranial sutures, expand the cranial cavity volume, and restore normal cranio-maxillofacial morphology. In recent years, surgical concepts and techniques have been continuously evolving. The main surgical procedures include endoscopic-assisted strip craniectomy for prematurely closed cranial sutures, cranial vault remodeling (such as the Pi procedure and traditional extensive calvarial vault incision, release, and remodeling), and spring-assisted cranial vault remodeling. Endoscopic-assisted strip craniectomy is suitable for infants diagnosed within 3 months of age. This procedure is minimally invasive and allows rapid recovery; however, postoperative cranial remodeling depends on helmet therapy. The Pi procedure and total cranial vault remodeling can achieve immediate and significant expansion of cranial cavity volume and morphological correction during the operation, and are currently the most widely used surgical procedures for children over 3 months old. Spring-assisted cranial vault remodeling achieves gradual expansion of the cranial cavity through continuous traction forces, but a second operation is required to remove the implanted devices. The selection of surgical procedures needs to comprehensively consider factors such as the child′s age, type of deformity, intracranial pressure level, and the technical conditions of the institution, and also relies on the evaluation and collaboration of a multidisciplinary team. Although NSC surgery is generally highly safe, during long-term follow-up, postoperative recurrence and skull defects are still the most critical and clinically significant complications. Abnormalities in the reossification process are regarded as the key mechanisms leading to these complications. Future research should, on the basis of clarifying the mechanism of postoperative reossification, further integrate individualized surgical planning, the application of new biomaterials, and the evaluation of long-term neurocognitive and quality-of-life outcomes, so as to promote the transformation of NSC treatment from morphological correction to long-term functional optimization.

Stroke, a cerebrovascular disease characterized by focal or global brain function impairment as its core clinical feature, is associated with high incidence, disability, and mortality rates. Its onset exhibits a certain circadian rhythmicity. With the acceleration of modern life rhythms and the development of science and technology, the prevalence of night-shift work and cross-time-zone travel has increased. Meanwhile, prolonged use of electronic products and extended entertainment time have led to an increase in the number of people with circadian rhythm disorders. Existing studies have confirmed that circadian rhythm disorders are significantly associated with the risk of various diseases, such as metabolic syndrome and cardiovascular and cerebrovascular diseases. However, the specific mechanisms remain unclear. Abnormal lipid metabolism is an important risk factor for stroke, especially ischemic stroke. The processes of lipid digestion, absorption, transport, synthesis, decomposition, and oxidation in the body are precisely regulated by central and peripheral molecular clocks, showing significant temporal characteristics. Circadian rhythm disorders are closely related to abnormal lipid metabolism and atherosclerosis. This article reviews the mechanisms by which circadian rhythms regulate lipid metabolism and their role in the onset and progression of stroke, and based on this, proposes new targets for stroke chronotherapy.

Antihyperglycemic agents include biguanides, α-glucosidase inhibitors (AGIs), thiazolidinediones (TZDs), insulin, dipeptidyl peptidase-Ⅳ (DPP-4) inhibitors, sodium-glucose cotransporter 2 (SGLT-2) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1RAs), glucokinase activators (GKAs) and peroxisome proliferator-activated receptor (PPAR) pan-agonists. Among them, the former four categories are traditional antihyperglycemic agents, while the latter five are novel antihyperglycemic agents. Studies have demonstrated that these agents not only exert effective glucose-lowering effects, but also exhibit potential in improving lipid metabolism, although their precise mechanisms remain to be further elucidated. Long-term chronic hyperglycemia in patients with type 2 diabetes mellitus (T2DM) disrupts lipid metabolic homeostasis via multiple pathophysiological pathways. Therefore, correcting lipid metabolism disorders has become one of the key objectives of T2DM management. However, in patients with T2DM complicated by lipid metabolism disorders, it is difficult to accurately select appropriate antihyperglycemic agents for treatment at the early stage of the disease. Based on this, this article reviews recent progress in the mechanism of the effects of different antihyperglycemic agents on lipid metabolism, and further explores their effects on lipid metabolism, so as to provide a reference for clinicians in selecting antihyperglycemic agents and help T2DM patients with lipid metabolism disorders achieve long-term clinical benefits.

Central nervous system (CNS) infections are common complications following neurosurgery, with bacteria being the predominant pathogens, while fungal infections are rare. This article reports the diagnosis and treatment of a patient with traumatic intracerebral hemorrhage who underwent craniotomy. One month after surgery, the patient developed unexplained fever, lethargy, and neck stiffness, raising a high clinical suspicion of CNS infection. However, conventional cerebrospinal fluid (CSF) routine and biochemical tests lacked specificity, and CSF culture was negative. Consequently, metagenomic next-generation sequencing (mNGS) of the CSF was performed. The mNGS results identified Pichia kudriavzevii (clinically known as Candida krusei). Based on the patient's clinical manifestations, signs, and auxiliary examination findings, a diagnosis of CNSinfection caused by Candida krusei was made. After more than 4 weeks of antifungal therapy with voriconazole, the patient′s condition improved and the patient was discharged. No recurrence was observed during follow-up. This case suggests that for CNS infections with atypical clinical presentations and nonspecific routine laboratory findings, mNGS can rapidly and accurately identify rare pathogens, providing a key basis for early targeted therapy and contributing to improved patient outcomes.